Face cooling increases blood pressure during central hypovolemia

A reduction in central blood volume can lead to cardiovascular decompensation (i.e., failure to maintain blood pressure). Cooling the forehead and cheeks using ice water raises blood pressure. Therefore, face cooling (FC) could be used to mitigate decreases in blood pressure during central hypovolemia. We tested the hypothesis that FC during central hypovolemia induced by lower-body negative pressure (LBNP) would increase blood pressure. Ten healthy participants (22 ± 2 yr, three women, seven men) completed two randomized LBNP trials on separate days. Trials began with 30 mmHg of LBNP for 6 min. Then, a 2.5-liter plastic bag of ice water (0 ± 0°C) (LBNP+FC) or thermoneutral water (34 ± 1°C) (LBNP+Sham) was placed on the forehead, eyes, and cheeks during 15 min of LBNP at 30 mmHg. Forehead temperature was lower during LBNP+FC than LBNP+Sham, with the greatest difference at 21 min of LBNP (11.1 ± 1.6 vs. 33.9 ± 1.4°C, P < 0.001). Mean arterial pressure was greater during LBNP+FC than LBNP+Sham, with the greatest difference at 8 min of LBNP (98 ± 15 vs. 80 ± 8 mmHg, P < 0.001). Cardiac output was higher during LBNP+FC than LBNP+Sham with the greatest difference at 18 min of LBNP (5.9 ± 1.4 vs. 4.9 ± 1.0 liter/min, P = 0.005). Forearm cutaneous vascular resistance was greater during LBNP+FC than LBNP+Sham, with the greatest difference at 15 min of LBNP (7.2 ± 3.4 vs. 4.9 ± 2.7 mmHg/perfusion units (PU), P < 0.001). Face cooling during LBNP increases blood pressure through increases in cardiac output and vascular resistance.

Endurance run increases circulating IL-6 and IL-1ra but downregulates ex vivo TNF-alpha and IL-1 beta production

This investigation determined the manner in which the cardiovascular system copes with the dehydration-induced reductions in cardiac output (Q) during prolonged exercise in the heat. On two separate occasions, seven endurance-trained subjects (maximal O2 consumption 4.70 +/- 0.41 l/min) cycled in the heat (35 degrees C) for 2 h, beginning at 62 +/- 2% maximal O2 consumption. During exercise, they randomly received either 0.2 liter of fluid and became dehydrated by 4.9 +/- 0.2% of their body weight [i.e., dehydration trial (DE)] or 3.6 +/- 0.4 liter of fluid and replaced 95% of fluid losses [i.e., euhydration trial (EU)]. During the 10- to 120-min period of EU, Q, mean arterial pressure (MAP), systemic vascular resistance (SVR), cutaneous vascular resistance (CVR), and plasma catecholamines did not change while esophageal temperature stabilized at 38.0 +/- 0.1 degrees C. Conversely, after 120 min of DE, Q and MAP were reduced 18 +/- 3 and 5 +/- 2%, respectively, compared with EU (P < 0.05). This was associated with a significantly higher SVR (17 +/- 6%) and plasma norepinephrine concentration (50 +/- 19%, P < 0.05). In addition, CVR was also significantly higher (126 +/- 16 vs. 102 +/- 6% of 20-min value; P < 0.05) during DE despite a 1.2 +/- 0.1 degrees C greater esophageal temperature (P < 0.05). In conclusion, significant reductions in Q are accompanied by significant increases in SVR and plasma norepinephrine and a slight although significant decline in MAP. The cutaneous circulation participates in this systemic vasoconstriction as indicated by increases in CVR despite significant hyperthermia.

Dehydration reduces cardiac output and increases systemic and cutaneous vascular resistance during exercise

This investigation determined the manner in which the cardiovascular system copes with the dehydration-induced reductions in cardiac output (Q) during prolonged exercise in the heat. On two separate occasions, seven endurance-trained subjects (maximal O2 consumption 4.70 +/- 0.41 l/min) cycled in the heat (35 degrees C) for 2 h, beginning at 62 +/- 2% maximal O2 consumption. During exercise, they randomly received either 0.2 liter of fluid and became dehydrated by 4.9 +/- 0.2% of their body weight [i.e., dehydration trial (DE)] or 3.6 +/- 0.4 liter of fluid and replaced 95% of fluid losses [i.e., euhydration trial (EU)]. During the 10- to 120-min period of EU, Q, mean arterial pressure (MAP), systemic vascular resistance (SVR), cutaneous vascular resistance (CVR), and plasma catecholamines did not change while esophageal temperature stabilized at 38.0 +/- 0.1 degrees C. Conversely, after 120 min of DE, Q and MAP were reduced 18 +/- 3 and 5 +/- 2%, respectively, compared with EU (P < 0.05). This was associated with a significantly higher SVR (17 +/- 6%) and plasma norepinephrine concentration (50 +/- 19%, P < 0.05). In addition, CVR was also significantly higher (126 +/- 16 vs. 102 +/- 6% of 20-min value; P < 0.05) during DE despite a 1.2 +/- 0.1 degrees C greater esophageal temperature (P < 0.05). In conclusion, significant reductions in Q are accompanied by significant increases in SVR and plasma norepinephrine and a slight although significant decline in MAP. The cutaneous circulation participates in this systemic vasoconstriction as indicated by increases in CVR despite significant hyperthermia.

Autonomic regulation of cutaneous vascular resistance in the bullfrog Rana catesbeiana

To gain a better understanding of the regulation of cutaneous blood flow in the bullfrog, the vascular innervation, vasoactivity and adrenoceptor types of the cutaneous vasculature were investigated using a pump-perfused skin preparation. Stimulation of cranial nerve I, the vagal ganglion, sympathetic ganglion 1 and sometimes sympathetic ganglion 2 caused cutaneous vascular resistance (CVR) to increase. Stimulation of cranial nerve IX and spinal nerves 1 and 2 had no effect on CVR. The response to stimulation of sympathetic ganglion 1 was antagonized by phentolamine but not by atropine. Phentolamine, atropine and alpha,beta-methylene ATP had no effect on the response to vagal stimulation. Both epinephrine (EPI) and norepinephrine (NE) increased CVR, with EPI being more potent than NE. The minimum concentrations of EPI and NE required for a significant change in CVR were much higher than plasma catecholamine levels reported for resting bullfrogs. Phentolamine antagonized, but propranolol had no effect on, the responses to the catecholamines. Isoproterenol caused small decreases in CVR which were abolished by propranolol. Acetylcholine was a weak vasodilator. The results indicate that the cutaneous vasculature has two types of vasomotor nerves: sympathetic nerves that are probably adrenergic, and other nerves that are non-adrenergic/non-cholinergic and which do not use ATP as a transmitter. Although catecholamines are vasoactive, the sensitivity of the cutaneous vasculature to EPI and NE is probably too low to allow a direct regulatory role of these hormones on CVR. There is no evidence for cholinergic regulation of CVR. Both alpha- and beta-adrenoceptors are present in the cutaneous vasculature. alpha-Adrenoceptors mediate the constrictor responses to sympathetic nerve stimulation and catecholamine administration. It is unlikely that beta-adrenoceptors play a significant role in regulating CVR.

Cutaneous Vascular Responses Evoked in the Hand by the Cold Pressor Test and by Mental Arithmetic

1. Laser Doppler flowmetry has been used to study changes in cutaneous erythrocyte flux produced in the hand (i) on successive immersion of the contralateral hand in water at 20°C (cold test) and then in water at 0–4°C (cold pressor test), and (ii) by mental arithmetic. 2. In 11 subjects, placing the right hand in water at 20°C for 2 min induced a significant decrease in cutaneous erythrocyte flux in the contralateral hand and a significant fall in mean arterial pressure. Cutaneous vascular resistance, calculated as arterial pressure/cutaneous erythrocyte flux, showed no significant change. Thus, the decrease in erythrocyte flux was apparently due to a fall in perfusion pressure. 3. Subsequent immersion of the right hand in water at 0–4°C for 2 min caused a significant decrease in erythrocyte flux in the contralateral hand and a significant rise in mean arterial pressure. It is concluded that the cold pressor response evoked from one hand elicited a substantial reflex vasoconstriction in the skin of the other hand; accordingly, calculated cutaneous vascular resistance increased significantly. 4. Eight subjects performed mental arithmetic for two periods of 2 min separated by a rest period of 2 min. By the end of the second minute of each period of mental arithmetic there was a significant decrease in erythrocyte flux. Mean arterial pressure increased significantly in the first period only, but calculated cutaneous vascular resistance increased in both periods, consistent with cutaneous vasoconstriction. 5. The cold pressor test and mental arithmetic are aversive stimuli that evoke the characteristic pattern of the alerting or defence response which includes splanchnic vasoconstriction and muscle vasodilatation. Previous studies on the cutaneous vascular component of this response have yielded equivocal results. The present study provides firm evidence that it includes cutaneous vasoconstriction, at least in the hand.

Effect of Morphine on Limb Capacitance and Resistance Vessels

1. The actions of 15 mg of intravenous morphine on hand and forearm capacitance and resistance vessels were studied with venous occlusion plethysmography. 2. In contrast to a 5% increase in forearm venous volume, intravenous morphine caused a 26% decrease in hand venous volume. This hand venoconstriction was confirmed by finding an increase in hand venous tone. The effects of morphine on hand veins were attenuated by intra-arterial phentolamine and blocked by intravenous naloxone. 3. Whereas morphine had no significant effect on forearm resistance vessels, it caused a 70% reduction in hand vascular resistance. 4. Intra-arterial morphine had no local action on hand capacitance or resistance vessels. 5. Though the contrasting actions of morphine on hand and forearm capacitance vessels resulted in no important change in limb venous capacitance, the large reduction of cutaneous vascular resistance may contribute to haemodynamic benefit in patients with pulmonary oedema.